MYH9, encoding the heavy chain of non-muscle myosin IIA, is a crucial gene. Non-muscle myosin IIA is involved in processes requiring intracellular chemomechanical force generation and actin cytoskeleton translocation. Its functions are regulated by phosphorylation of light and heavy chains and interactions with other proteins. It plays a role in embryonic development and is associated with multiple biological processes [1].

MYH9-related diseases are caused by its mutations, following an autosomal-dominant pattern. These diseases include macrothrombocytopenia, leukocyte inclusions, and risks of renal failure, hearing loss, and cataracts [2]. In tumors, MYH9 has dual functions. In hepatocellular carcinoma, it promotes tumor stemness by interacting with GSK3β and reducing its protein expression, and HBX can induce MYH9 expression [3]. In gastric cancer, nuclear MYH9 promotes metastasis by inducing CTNNB1 transcription [4]. In rheumatoid arthritis, MYH9 promotes synoviocyte migration and invasion [5].

In conclusion, MYH9 is essential for generating intracellular force and actin-related processes. Its mutations lead to MYH9-related diseases. In addition, MYH9 is closely associated with tumor progression and some autoimmune diseases. Studies on MYH9-related KO or CKO mouse models (not specifically mentioned in provided references but valuable in general gene-function studies) could further clarify its role in these disease conditions, providing potential therapeutic targets for relevant diseases.